Explore the vast range of titles available.

Cardiovascular disease remains the leading cause of disease burden globally, which underlies the continuing need to identify new complementary targets for prevention. Over the past 5-10 years, the pooling of multiple data sets into 'mega-studies' has accelerated progress in research on stress as a risk and prognostic factor for cardiovascular disease. Severe stressful experiences in childhood, such as physical abuse and household substance abuse, can damage health and increase the risk of multiple chronic conditions in adulthood. Compared with childhood stress and adulthood classic risk factors, such as smoking, high blood pressure, and high serum cholesterol levels, the harmful effects of stress in adulthood are generally less marked. However, adulthood stress has an important role as a disease trigger in individuals who already have a high atherosclerotic plaque burden, and as a determinant of prognosis and outcome in those with pre-existing cardiovascular or cerebrovascular disease. In real-life settings, mechanistic studies have corroborated earlier laboratory-based observations on stress-related pathophysiological changes that underlie triggering, such as lowered arrhythmic threshold and increased sympathetic activation with related increases in blood pressure, as well as pro-inflammatory and procoagulant responses. In some clinical guidelines, stress is already acknowledged as a target for prevention for people at high overall risk of cardiovascular disease or with established cardiovascular disease. However, few scalable, evidence-based interventions are currently available.

White matter hyperintensities (WMH) are frequently divided into periventricular (PWMH) and deep (DWMH), and the two classes have been associated with different cognitive, microstructural, and clinical correlates. However, although this distinction is widely used in visual ratings scales, how to best anatomically define the two classes is still disputed. In fact, the methods used to define PWMH and DWMH vary significantly between studies, making results difficult to compare. The purpose of this study was twofold: first, to compare four current criteria used to define PWMH and DWMH in a cohort of healthy older adults (mean age: 69.58 ± 5.33 years) by quantifying possible differences in terms of estimated volumes; second, to explore associations between the two WMH sub-classes with cognition, tissue microstructure and cardiovascular risk factors, analysing the impact of different criteria on the specific associations. Our results suggest that the classification criterion used for the definition of PWMH and DWMH should not be considered a major obstacle for the comparison of different studies. We observed that higher PWMH load is associated with reduced cognitive function, higher mean arterial pressure and age. Higher DWMH load is associated with higher body mass index. PWMH have lower fractional anisotropy than DWMH, which also have more heterogeneous microstructure. These findings support the hypothesis that PWMH and DWMH are different entities and that their distinction can provide useful information about healthy and pathological aging processes. •Classification criteria for periventricular/deep white matter hyperintensities are compared.•The definition of PWMH and DWMH is not a major obstacle for study comparison.•PWMH and DWMH have different functional, microstructural and clinical correlates.•10mm distance rule gave best separation in terms of associations with the tested factors.

Sleep dysregulation is a feature of dementia but it remains unclear whether sleep duration prior to old age is associated with dementia incidence. Using data from 7959 participants of the Whitehall II study, we examined the association between sleep duration and incidence of dementia (521 diagnosed cases) using a 25-year follow-up. Here we report higher dementia risk associated with a sleep duration of six hours or less at age 50 and 60, compared with a normal (7 h) sleep duration, although this was imprecisely estimated for sleep duration at age 70 (hazard ratios (HR) 1.22 (95% confidence interval 1.01–1.48), 1.37 (1.10–1.72), and 1.24 (0.98–1.57), respectively). Persistent short sleep duration at age 50, 60, and 70 compared to persistent normal sleep duration was also associated with a 30% increased dementia risk independently of sociodemographic, behavioural, cardiometabolic, and mental health factors. These findings suggest that short sleep duration in midlife is associated with an increased risk of late-onset dementia. Sleep dysregulation has been linked to dementia, but it is unknown whether sleep duration earlier in life is associated with dementia risk. Here, the authors show higher dementia risk associated with short sleep duration (six hours or less) in a longitudinal study of middle and older age adults.

The role of obesity and overweight in occurrence of COVID-19 is unknown. We conducted a large-scale general population study using data from a community-dwelling sample in England (n = 334,329; 56.4 ±8.1 y; 54.5% women) with prospective linkage to national registry on hospitalization for COVID-19. Body mass index (BMI, from measured height and weight) was used as an indicator of overall obesity, and waist–hip ratio for central obesity. Main outcome was cases of COVID-19 serious enough to warrant a hospital admission from 16 March 2020 to 26 April 2020. Around 0.2% (n = 640) of the sample were hospitalized for COVID-19. There was an upward linear trend in the likelihood of COVID-19 hospitalization with increasing BMI, that was evident in the overweight (odds ratio, 1.39; 95% CI 1.13 to 1.71; crude incidence 19.1 per 10,000) and obese stage I (1.70;1.34 to 2.16; 23.3 per 10,000) and stage II (3.38; 2.60 to 4.40; 42.7 per 10,000) compared to normal weight (12.5 per 10,000). This gradient was little affected after adjustment for a wide range of covariates; however, controlling for biomarkers, particularly high-density lipoprotein cholesterol and glycated hemoglobin, led to a greater degree of attenuation. A similar pattern of association emerged for waist–hip ratio. In summary, overall and central obesity are risk factors for COVID-19 hospital admission. Elevated risk was apparent even at modest weight gain. The mechanisms may involve impaired glucose and lipid metabolism.

Objective To examine the role of psychological distress (anxiety and depression) as a potential predictor of site specific cancer mortality. Design Pooling of individual participant data from 16 prospective cohort studies initiated 1994-2008.Setting Nationally representative samples drawn from the health survey for England (13 studies) and the Scottish health survey (three studies).Participants 163 363 men and women aged 16 or older at study induction, who were initially free of a cancer diagnosis, provided self reported psychological distress scores (based on the general health questionnaire, GHQ-12) and consented to health record linkage.Main outcome measure Vital status records used to ascertain death from 16 site specific malignancies; the three Scottish studies also had information on cancer registration (incidence).Results The studies collectively contributed an average of 9.5 years of mortality surveillance during which there were 16 267 deaths (4353 from cancer). After adjustment for age, sex, education, socioeconomic status, body mass index (BMI), and smoking and alcohol intake, and with reverse causality (by left censoring) and missing data (by imputation) taken into account, relative to people in the least distressed group (GHQ-12 score 0-6), death rates in the most distressed group (score 7-12) were consistently raised for cancer of all sites combined (multivariable adjusted hazard ratio 1.32, 95% confidence interval 1.18 to 1.48) and cancers not related to smoking (1.45, 1.23 to 1.71), as well as carcinoma of the colorectum (1.84, 1.21 to 2.78), prostate (2.42, 1.29 to 4.54), pancreas (2.76, 1.47 to 5.19), oesophagus (2.59, 1.34 to 5.00), and for leukaemia (3.86, 1.42 to 10.5). Stepwise associations across the full range of distress scores were observed for colorectal and prostate cancer.Conclusion This study contributes to the growing evidence that psychological distress might have some predictive capacity for selected cancer presentations, in addition to other somatic diseases.

Psychological stress is thought to contribute to the cardiovascular disease process at several stages, including the long-term development of coronary heart disease and acute triggering of cardiac events. In this Review, Steptoe and Kivimäki summarize the evidence for the association between stress and cardiovascular disease, with a focus on external work-related and social stressors. They also discuss the effects of stress-management strategies on cardiovascular health. The physiological reaction to psychological stress, involving the hypothalamic–pituitary–adrenocortical and sympatho–adrenomedullary axes, is well characterized, but its link to cardiovascular disease risk is not well understood. Epidemiological data show that chronic stress predicts the occurrence of coronary heart disease (CHD). Employees who experience work-related stress and individuals who are socially isolated or lonely have an increased risk of a first CHD event. In addition, short-term emotional stress can act as a trigger of cardiac events among individuals with advanced atherosclerosis. A stress-specific coronary syndrome, known as transient left ventricular apical ballooning cardiomyopathy or stress (Takotsubo) cardiomyopathy, also exists. Among patients with CHD, acute psychological stress has been shown to induce transient myocardial ischemia and long-term stress can increase the risk of recurrent CHD events and mortality. Applications of the 'stress concept' (the understanding of stress as a risk factor and the use of stress management) in the clinical settings have been relatively limited, although the importance of stress management is highlighted in European guidelines for cardiovascular disease prevention. Key Points Psychological stress contributes to cardiovascular disease at several stages, including the long-term development of coronary heart disease and acute triggering of cardiac events Disturbances of inflammatory, hemostatic, and autonomic processes are likely to be the mechanisms by which short-term psychological stress triggers acute myocardial infarction Chronic stress at work and in private life is associated with a 40–50% increase in the occurrence of coronary heart disease in prospective observational studies Indicators of elevated long-term stress, such as social isolation and work-related stress, are associated with poor prognosis among patients with established coronary heart disease Stress-management interventions improve the quality of life of patients with advanced coronary heart disease, but effects on disease prognosis have been inconsistent

Information and assurance from healthcare workers (HCWs) is reported by laypeople as a key factor in their decision to get vaccinated. However, previous research has shown that, as in the general population, hesitancy towards vaccines exists among HCWs as well. Previous studies further suggest that HCWs with a higher confidence in vaccinations and vaccine providers are more willing to take the vaccines themselves and to recommend vaccines to patients. In the present study with 2962 Finnish HCWs (doctors, head nurses, nurses, and practical nurses), we explored the associations between HCWs' vaccination confidence (perceived benefit and safety of vaccines and trust in health professionals), their decisions to accept vaccines for themselves and their children, and their willingness to recommend vaccines to patients. The results showed that although the majority of HCWs had high confidence in vaccinations, a notable share reported low vaccination confidence. Moreover, in line with previous research, HCWs with higher confidence in the benefits and safety of vaccines were more likely to accept vaccines for their children and themselves, and to recommend vaccines to their patients. Trust in other health professionals was not directly related to vaccination or recommendation behavior. Confidence in the benefits and safety of vaccines was highest among doctors, and increased along with the educational level of the HCWs, suggesting a link between confidence and the degree of medical training. Ensuring high confidence in vaccines among HCWs may be important in maintaining high vaccine uptake in the general population.

ObjectiveTo examine whether social isolation and loneliness (1) predict acute myocardial infarction (AMI) and stroke among those with no history of AMI or stroke, (2) are related to mortality risk among those with a history of AMI or stroke, and (3) the extent to which these associations are explained by known risk factors or pre-existing chronic conditions.MethodsParticipants were 479 054 individuals from the UK Biobank. The exposures were self-reported social isolation and loneliness. AMI, stroke and mortality were the outcomes.ResultsOver 7.1 years, 5731 had first AMI, and 3471 had first stroke. In model adjusted for demographics, social isolation was associated with higher risk of AMI (HR 1.43, 95% CI 1.3 to –1.55) and stroke (HR 1.39, 95% CI 1.25 to 1.54). When adjusted for all the other risk factors, the HR for AMI was attenuated by 84% to 1.07 (95% CI 0.99 to 1.16) and the HR for stroke was attenuated by 83% to 1.06 (95% CI 0.96 to 1.19). Loneliness was associated with higher risk of AMI before (HR 1.49, 95% CI 1.36 to 1.64) but attenuated considerably with adjustments (HR 1.06, 95% CI 0.96 to 1.17). This was also the case for stroke (HR 1.36, 95% CI 1.20 to 1.55 before and HR 1.04, 95% CI 0.91 to 1.19 after adjustments). Social isolation, but not loneliness, was associated with increased mortality in participants with a history of AMI (HR 1.25, 95% CI 1.03 to 1.51) or stroke (HR 1.32, 95% CI 1.08 to 1.61) in the fully adjusted model.ConclusionsIsolated and lonely persons are at increased risk of AMI and stroke, and, among those with a history of AMI or stroke, increased risk of death. Most of this risk was explained by conventional risk factors.

AbstractObjectiveTo compare established associations between risk factors and mortality in UK Biobank, a study with an exceptionally low rate of response to its baseline survey, against those from representative studies that have conventional response rates.DesignProspective cohort study alongside individual participant meta-analysis of other cohort studies.SettingUnited Kingdom.ParticipantsAnalytical sample of 499 701 people (response rate 5.5%) in analyses in UK Biobank; pooled data from the Health Surveys for England (HSE) and the Scottish Health Surveys (SHS), including 18 studies and 89 895 people (mean response rate 68%). Both study populations were linked to the same nationwide mortality registries, and the baseline age range was aligned at 40-69 years.Main outcome measureDeath from cardiovascular disease, selected malignancies, and suicide. To quantify the difference between hazard ratios in the two studies, a ratio of the hazard ratios was used with HSE-SHS as the referent.ResultsRisk factor levels and mortality rates were typically more favourable in UK Biobank participants relative to the HSE-SHS consortium. For the associations between risk factors and mortality endpoints, however, close agreement was seen between studies. Based on 14 288 deaths during an average of 7.0 years of follow-up in UK Biobank and 7861 deaths over 10 years of mortality surveillance in HSE-SHS, for cardiovascular disease mortality, for instance, the age and sex adjusted hazard ratio for ever having smoked cigarettes (versus never) was 2.04 (95% confidence interval 1.87 to 2.24) in UK Biobank and 1.99 (1.78 to 2.23) in HSE-SHS, yielding a ratio of hazard ratios close to unity (1.02, 0.88 to 1.19). The overall pattern of agreement between studies was essentially unchanged when results were compared separately by sex and when baseline years and censoring dates were aligned.ConclusionDespite a very low response rate, risk factor associations in the UK Biobank seem to be generalisable.

With depression being the psychiatric disorder incurring the largest societal costs in developed countries, there is a need to gather evidence on the role of nutrition in depression, to help develop recommendations and guide future psychiatric health care. The aim of this systematic review was to synthesize the link between diet quality, measured using a range of predefined indices, and depressive outcomes. Medline, Embase and PsychInfo were searched up to 31st May 2018 for studies that examined adherence to a healthy diet in relation to depressive symptoms or clinical depression. Where possible, estimates were pooled using random effect meta-analysis with stratification by observational study design and dietary score. A total of 20 longitudinal and 21 cross-sectional studies were included. These studies utilized an array of dietary measures, including: different measures of adherence to the Mediterranean diet, the Healthy Eating Index (HEI) and Alternative HEI (AHEI), the Dietary Approaches to Stop Hypertension, and the Dietary Inflammatory Index. The most compelling evidence was found for the Mediterranean diet and incident depression, with a combined relative risk estimate of highest vs. lowest adherence category from four longitudinal studies of 0.67 (95% CI 0.55–0.82). A lower Dietary Inflammatory Index was also associated with lower depression incidence in four longitudinal studies (relative risk 0.76; 95% CI: 0.63–0.92). There were fewer longitudinal studies using other indices, but they and cross-sectional evidence also suggest an inverse association between healthy diet and depression (e.g., relative risk 0.65; 95% CI 0.50–0.84 for HEI/AHEI). To conclude, adhering to a healthy diet, in particular a traditional Mediterranean diet, or avoiding a pro-inflammatory diet appears to confer some protection against depression in observational studies. This provides a reasonable evidence base to assess the role of dietary interventions to prevent depression. This systematic review was registered in the PROSPERO International Prospective Register of Systematic Reviews under the number CRD42017080579.